Pericoronary inflammation by coronary CT angiography is associated with plaque vulnerability in chronic non-obstructive coronary artery disease

Background Pericoronary inflammation is associated with a low attenuation plaque phenotype vulnerable to plaque rupture and may represent a risk marker in coronary artery disease (CAD). However, the predictive role of pericoronary inflammation in chronic non-obstructive CAD is not well established. Purpose To explore the association between pericoronary inflammation and coronary artery plaque vulnerability by coronary CT angiography (CCTA) in chronic non-obstructive CAD. Methods We included 1067 patients identified from the Norwegian Registry of Invasive Cardiology (NORIC) with chronic non-obstructive CAD diagnosed by CCTA. Plaque burden, plaque composition and pericoronary adipose tissue (PCAT) attenuation were assessed on CCTA using a novel semiautomatic software in six main coronary artery segments (Figure 1, A). Plaque burden was quantified as percentage of vessel volume, and plaque subtypes classified by attenuation thresholds in Hounsfield Units (HU) as necrotic core (-30 to 75 HU), fibrofatty (76 to 130 HU), fibrous (131 to 350 HU) or calcified (>350 HU). Low attenuating plaques (≤130 HU) were defined as vulnerable. Mean segmental PCAT attenuation ≥−70.1 HU indicated pericoronary inflammation. High pericoronary inflammatory burden was defined as exhibiting higher than median number of inflamed segments (≥2 segments with PCAT ≥−70.1 HU; Figure 1, B). Results In the total study cohort (median age 63 years [IQR 57-70], 48% women) a high pericoronary inflammatory burden was detected in 62% of patients. Patients with high inflammatory burden were younger (61 [52–69] vs. 66 [58–72] years), less often women (44% vs. 50%) and smokers (16% vs. 21%), had higher BMI (28 [25–31] vs. 26 [23–29] kg/m²) and were more frequently obese (31% vs. 16%) (all p<0.05). Other cardiovascular risk factors were similar between groups. Patients with high pericoronary inflammatory burden exhibited increased low-attenuating vulnerable plaque burden, reflected by greater fibrofatty and necrotic core components and less dense calcium, whereas total plaque burden and fibrous plaque did not differ between groups (Figure 1, C). In multivariable linear regression analyses adjusting for traditional risk factors, calcium score and total plaque burden, higher inflammatory burden (b= 0.75, 95% CI [0.45-1.06], p<0.001) was independently associated with low attenuating plaque burden. Conclusion In non-obstructive CAD, a high pericoronary inflammatory burden is associated with a low attenuating plaque phenotype vulnerable to rupture and may predispose to acute cardiac events. Figure 1. A) The six main coronary artery segments on CCTA. B) Axial CCTA image of LAD showing low PCAT attenuation and more calcified plaque (left) and high PCAT attenuation and less calcified plaque (right). C) Table showing plaque composition in percent of vessel volume for all main segments, grouped by low vs. high pericoronary inflammatory burden.